Obesity Itself Not Diabetes Risk

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Having excess visceral fat and insulin resistance, but not being obese in and of itself, appears to put heavier patients at risk for prediabetes and diabetes, researchers found.

Point out that there were no associations between prediabetes or diabetes incidence with general markers of obesity, such as body mass index (BMI) or total body fat.

Having excess visceral fat and insulin resistance -- but not being obese in and of itself -- appears to put heavier patients at risk for prediabetes and diabetes, researchers found.

Among obese adults, visceral fat was associated with more than a twofold increased risk of developing incident diabetes (odds ratio 2.42, 95% CI 1.59 to 3.68), according to James de Lemos, MD, of the University of Texas Southwestern Medical Center in Dallas, Texas, and colleagues.

And developing either condition was also associated with markers of insulin resistance, including elevated fructosamine levels (OR 1.95, 95% CI 1.43 to 2.67) and elevated fasting blood glucose (OR 1.88, 95% CI 1.38 to 2.56), they wrote in an obesity-themed issue of the Journal of the American Medical Association.

But there were no associations with general markers of obesity, including body mass index (BMI) or total body fat.

"Our study may have implications for understanding differences between metabolically healthy and pathologic obesity," they wrote.

The risk of developing type 2 diabetes is heterogeneous among obese patients, and factors that discriminate risk of developing the condition haven't been well studied.

So the authors looked at associations between prediabetes and diabetes and baseline adipose tissue distribution, adipokines, lipids, biomarkers of insulin resistance, as well as family history of diabetes and factors at follow-up in "a multiethnic cohort of obese adults [≤30 kg/m2] with extensive cardiovascular, metabolic, and adipose tissue phenotyping" enrolled in the Dallas Heart Study from 2000 to 2002.

A total of 732 participants received multiple surveys, laboratory testing, and imaging studies. Fasting blood glucose was sampled in a subgroup of 512 participants at baseline.

Again, there was no association with measures of general adiposity, they reported.

At a press briefing Tuesday, de Lemos noted that there was no simple way to determine whether body fat was subcutaneous or visceral without imaging studies.

He noted that the association of weight gain at follow-up with diabetes was of particular significance because "if obese individuals are unable to lose significant amounts of weight, if we can prevent additional weight gain over follow-up, we can do a lot to reduce the risk of the development of diabetes."

He also suggested prospective treatments could transfer visceral fat to the subcutaneous region.

The authors concluded that "a dysfunctional adiposity phenotype, characterized by excess visceral fat and biomarkers of insulin resistance," was independently associated with development of prediabetes and diabetes, and said their findings suggest that "clinically measurable markers of adipose tissue distribution and insulin resistance may be useful in prediabetes and diabetes risk discrimination among obese individuals."

The researchers noted that the number of diabetes events were modest, and time to diabetes or prediabetes onset was not measured. They also said the study was limited by a lack of generalizability and missing glucose tolerance testing and measures of average blood glucose in the Dallas cohort.

The study was supported by the Donald W. Reynolds Foundation and the U.S. Public Health Service General Clinical Research Center, as well as the NIH, Alere, and Roche Diagnostics.

de Lemos received support from Roche Diagnostics, Abbott Diagnostics, Alere, Bristol-Myers Squibb, and sanofi-aventis. He acted as a consultant for Tethys Bioscience, AstraZeneca, Daiichi Sankyo. One co-author acted as a consultant for F. Hoffmann LaRoche, Genentech, sanofi-aventis, Daiichi Sankyo, Novo Nordisk, and Tethys Bioscience. Another was supported by the National Heart, Lung, and Blood Institute. And yet another was supported by the NIH.

Reviewed by Robert Jasmer, MD Associate Clinical Professor of Medicine, University of California, San Francisco and Dorothy Caputo, MA, BSN, RN, Nurse Planner

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